Dynorphin-(1–13)-Like Immunoreactivity in Central Nervous System and Pituitary Gland of Spontaneously Hypertensive Rats

Kouchich, F. J.; Quock, Raymond M.; Tseng, Leon F.

doi:10.3109/10641968409044031

Cited by 13 publications

(2 citation statements)

References 28 publications

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“…In general, the reports show that DN-A (both 1 -8 and 1-13) levels in SHR with fully developed hypertension are consid erably less than those of SHR in various brainstem and hypothalamic nuclei and in the neurointermediate pituitary [10,12,15]. The findings of Conway et al [ 11 ] are opposed, in that no changes in DN-A levels were found in a variety of brainstem and hypothalamic nu clei of 14-week-old SHR compared to WKY.…”

Section: Discussioncontrasting

confidence: 46%

Age-Related Changes in Opioid Peptide Concentrations in Brain and Pituitary of Spontaneously Hypertensive Rats

Wong

Hong

et al. 1992

Pharmacology

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The relationship of age-dependent changes in concentrations of various opioid peptides in the brain and pituitary to the development of hypertension was studied in the spontaneously hypertensive rat (SHR). Normotensive Wistar-Kyoto (WKY) and Sprague-Dawley rats served as controls. Opioids determined were dynorphin A (1-8) [DN-A(1–8)], β-endorphin (BE) and Met-enkephalin (ME). Three approaches were used: (1) temporal correlations of opioid concentrations with the onset of hypertension in 4-, 8-, 12- and 16-week-old rats; (2) study of opioid changes when hypertension development was prevented with antihypertensive drugs and (3) determination of possible opioid peptide changes in another rat model of hypertension, the deoxycorticosterone acetate (DOCA) + salt model. Opioid peptide concentration differences (SHR/ WKY) found were as follows. There were much lower DN-A(1–8) levels in the SHR hippocampus and hypothalamus at all ages studied. At 12 and 16 weeks, coincidently with the onset of hypertension, lower levels of BE were found in the anterior lobe of the pituitary, but there were higher BE and ME levels found in the neurointermediate lobe (NIL). Prevention of hypertension in SHR by 8 weeks of oral therapy with guanethidine and hydralazine reversed the BE and ME changes in the NIL but not in the anterior lobe. There were no brain or pituitary changes in opioid peptide concentrations associated with DOCA-salt hypertension. The results are interpreted as supporting a role for altered concentrations of brain and pituitary opioids in the genesis of SHR hypertension.

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Section: Discussioncontrasting

confidence: 46%

Age-Related Changes in Opioid Peptide Concentrations in Brain and Pituitary of Spontaneously Hypertensive Rats

Wong

Hong

et al. 1992

Pharmacology

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“…Hypertension is associated with significant changes in the opioid system, and physiological interaction between cardiovascular and pain-modulating systems has been demonstrated (Randich & Maixner 1984). Alterations in the brain opioid receptors in both experimental and genetic hypertension have been found (Zamir et al , 1981Bhargava & Das 1986), and levels of endogenous opioids like betaendorphin (Hutchinson et al 198 l), met-enkephalin (Nakamura & Kayashi 1982) and dynorphin (1-13) (Kouchich et al 1984) appear to be different in the tissues of normotensive and hypertensive rats. Therefore, endogenous opioid peptides are thought to play a role in the generation of chronically elevated arterial pressure (Dworkin et al 1978;Julius &Johnson 1985).…”

Section: E Widy-tyszkiewicz and A Czdonkowskimentioning

confidence: 99%

Normotensive Wistar Rats Differ From Spontaneously Hypertensive and Renal Hypertensive Rats in Their Cardiovascular Responses to Opioid Agonists

Tyszkiewicz

Członkowski

1991

Clin Exp Pharma Physio

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1. The effects of three opioid receptor agonists on the blood pressure and heart rate of anaesthetized normotensive, spontaneously hypertensive and renal hypertensive rats were measured. 2. Mu agonist morphiceptin i.c.v. induced a pressor response and increase in heart rate in hypertensive rats, but hypotension in normotensive rats. After intravenous (i.v.) injection, morphiceptin produced a hypotensive response in all three groups of rats. 3. In contrast, the delta agonist DTLET i.c.v. decreased blood pressure and heart rate in hypertensive rats, but increased both pressure and beat rate in normotensive rats. After i.v. injections DTLET produced a hypertensive response and increase in heart rate in all groups of rats. 4. Kappa agonist U-50, 488H given i.c.v. induced effects similar to morphiceptin: an increase in blood pressure and heart rate in hypertensive and a decrease in normotensive rats. After i.v. injections U-50, 488H produced decreases in blood pressure and heart rate in all treated groups of rats. 5. Pretreatment with naloxone antagonized the activity of morphiceptin but prevented only the stimulating effect of DTLET in normotensive rats. Cardiovascular actions of U-50, 488H were not blocked by naloxone. 6. The results suggest that opioid agonists exert similar changes in cardiovascular function at central and peripheral sites in both models of experimental hypertension and these effects are different in normotensive rats.

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Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity

Słowińska-Srzednicka

Zgliczyński

Soszyński

et al. 1988

Eur J Clin Pharmacol

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The role of alpha 2-adrenoceptor stimulation by clonidine on the secretion of beta-endorphin, ACTH, and cortisol in essential hypertension and obesity was studied in 45 subjects: 15 non-obese hypertensives, 10 obese hypertensives, 11 obese normotensives, and 9 healthy subjects. The circadian rhythm of plasma beta-endorphin, ACTH, and cortisol was determined after placebo and after three days on clonidine 0.45 mg daily. Clonidine lowered the blood pressure and blood ACTH and cortisol levels in all the subjects. A significant decrease in beta-endorphin after clonidine occurred in the healthy subjects. In obese normotensives basal beta-endorphin concentrations were significantly higher than in healthy subjects and did not change after clonidine. In about 50% of non-obese and obese hypertensives a significant increase in beta-endorphin secretion after clonidine was noted (responders). In the subgroup of non-obese hypertensive responders no circadian rhythm of beta-endorphin was observed. The results suggest that adrenergic regulation of beta-endorphin secretion is altered in obesity and in certain patients with essential hypertension.

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Dynorphin-(1–13)-Like Immunoreactivity in Central Nervous System and Pituitary Gland of Spontaneously Hypertensive Rats

Cited by 13 publications

References 28 publications

Age-Related Changes in Opioid Peptide Concentrations in Brain and Pituitary of Spontaneously Hypertensive Rats

Age-Related Changes in Opioid Peptide Concentrations in Brain and Pituitary of Spontaneously Hypertensive Rats

Normotensive Wistar Rats Differ From Spontaneously Hypertensive and Renal Hypertensive Rats in Their Cardiovascular Responses to Opioid Agonists

Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity

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